Placental Immunology, Viviparity, Evolution

The immunological defences of vertebrates are based on two systems, the innate [non specific] and the adaptive [specific ]. The innate uses largely monocytes, macrophages, granulocytes, NK [natural killer] and mast cells, with complement and acute phase proteins as humoral effectors. This is integrated with the adaptive system which employs the MHC controlled T and B lymphocytes and humoral antibodies. The innate is more primitive but both had evolved at least 220 million years ago [mya]. Vertebrate matrotrophic viviparity, based on internal fertilisation, retention of an allogeneic conceptus, and the development of a placenta in the uterus evolved 150–100 mya and was therefore always constrained by immunological considerations (Sacks et al. 1999; Parham 2004). These include the need for local tolerance in the uterus but maintenance of a normal level of systemic immunological surveillance.

Initially the brief toleration of the spermatozoa and seminal fluid components is based on the uterine epithelium providing a significant cellular barrier together with the local immunomodulation by the progesterone secretion from the corpus luteum developed from the ovulated ovarian follicle. After fertilisation the laying down of a shell around the zygote will provide a solely maternally derived immunological camouflage. Retention of the shelled yolky egg for ovoviviparity could probably be ignored immunologically, as in the monotremes.